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Control of adipose tissue cellularity by the terminal complement cascade

Nature Reviews Endocrinology volume 19, pages 679–680 (2023)Cite this article

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Adipocytes have high levels of many components of the complement system. These components are involved in antimicrobial activities, but also have the potential to regulate the maintenance and turn-over of adipocytes under normal and pathophysiological conditions through positive and negative regulation of the membrane attack complex.

It is widely accepted that members of the complement pathway are expressed at high levels in white adipose tissue (WAT). Terminal stages of this pathway are related to the production of membrane attack complexes (MACs). MACs cause lysis of pathogens and can also lead to autolysis of the host cells. Cellular lysis is counteracted by different cellular defence mechanisms that control this ‘tug-of-war’ behaviour of the complement system: it can be kept in check or let loose and activate a cell death pathway. The broad versatility of activation and suppression processes enables a high level of adaptation to different scenarios. The role of the complement system in normal adipose tissue homeostasis has gone largely unnoticed; evidence suggests this process has highly important roles, ranging from the development of hypertrophic WAT to lipodystrophy.

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Fig. 1: Regulation of the membrane attack complex.

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Acknowledgements

The authors were supported by US National Institutes of Health Grants R01-DK55758, R01-DK127274, R01-DK131537, R01-DK099110, P01-AG051459 and RC2-DK118620 (to P.E.S).

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  1. Scientific Department, Wellcomet GmbH, Karlsruhe, Germany

    Ilja L. Kruglikov

  2. Touchstone Diabetes Center, University of Texas Southwestern Medical Center, Dallas, TX, USA

    Philipp E. Scherer

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  1. Ilja L. Kruglikov
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  2. Philipp E. Scherer
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Correspondence to Philipp E. Scherer.

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Kruglikov, I.L., Scherer, P.E. Control of adipose tissue cellularity by the terminal complement cascade. Nat Rev Endocrinol 19, 679–680 (2023). https://doi.org/10.1038/s41574-023-00900-w

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